Is sugar addictive

Relevant literature on sugar as a drug/ reward

    • Serge Ahmed (2013) Sugar addiction: pushing the drug-sugar analogy to the limit. In: Curr Opin Clin Nutr Metab Care. 2013 Jul;16(4):434-9. doi: 10.1097/MCO.0b013e328361c8b8.
      • “Available evidence in humans shows that sugar and sweetness can induce reward and craving that are comparable in magnitude to those induced by addictive drugs. … sugar and sweet reward can not only substitute to addictive drugs, like cocaine, but can even be more rewarding and attractive. At the neurobiological level, the neural substrates of sugar and sweet reward appear to be more robust than those of cocaine …”
    • M.N. Avena et al. (2011) Sucrose sham feeding on a binge schedule releases accumbens dopamine repeatedly and eliminates the acetylcholine satiety response. In: Neuroscience. 2006; 139(3):813-20. Epub 2006 Feb 7
      • “In conclusion, the taste of sugar can increase extracellular dopamine in the nucleus accumbens without fail in animals on a dietary regimen that causes bingeing and sugar dependency. During sham feeding, the acetylcholine satiation signal is eliminated, and the animals drink more. These findings support the hypothesis that dopamine is released repeatedly in response to taste when bingeing on sweet food, and the acetylcholine satiety effect is greatly reduced by purging; this may be relevant to bulimia nervosa in humans.”
    • M.N. Avena et al. (2008) Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. In: Neurosci Biobehav Rev. 2008; 32(1): 20–39.
      • “The reviewed evidence supports the theory that, in some circumstances, intermittent access to sugar can lead to behavior and neurochemical changes that resemble the effects of a substance of abuse. According to the evidence in rats, intermittent access to sugar and chow is capable of producing a “dependency”.”
    • Paul Klenowski et al. (2016) Prolonged Consumption of Sucrose in a Binge-Like Manner, Alters the Morphology of Medium Spiny Neurons in the Nucleus Accumbens Shell. In: Front Behav Neurosci. 2016; 10: 54.
      • “In terms of long-term sucrose consumption, we observed an increase in spine density similar to amphetamine, cocaine and nicotine and opposite to the effect of morphine. However, unlike amphetamine and cocaine, but similar to nicotine, the increase of spine density on long-term exposure to sucrose is limited to the NAc shell. …  Taken together, this posits sucrose as a potent modulator of neuron morphology following prolonged heavy use, which is akin to the effects observed from drugs of abuse. … The results from this study add merit to the hypothesis that sugars such as sucrose potentially have addictive properties following long-term, binge-like consumption. Our results also have implications for the growing number of children and adolescents who maintain unhealthy eating habits (high sugar consumption and binge eating) into adulthood. In line with the increased risk of developing metabolic effects it is also possible that neurological and psychiatric consequences affecting mood and motivation may also result from these behaviors.”
    • Quingying Meng et al. (2016) Systems Nutrigenomics Reveals Brain Gene Networks Linking Metabolic and Brain Disorders. In: EBioMedicineVolume 7, May 2016, Pages 157–166.
      • Interpretation in UCLA Newsroom: Fructose alters hundreds of brain genes, which can lead to a wide range of diseases (2016), http://newsroom.ucla.edu/releases/fructose-alters-hundreds-of-brain-genes-which-can-lead-to-a-wide-range-of-diseases: High fructose intake by rats changed at first two genes in their brains and then, through these changes, more than 700 genes in the hypothalamus (the brain’s major metabolic control center) and more than 200 genes in the hippocampus (which helps regulate learning and memory). This led to memory impairment, much higher blood glucose, triglycerides and insulin levels. “Those results are significant because in humans, elevated glucose, triglycerides and insulin are linked to obesity, diabetes and many other diseases.”
    • Allison M. Meyers, Devry Mourra, Jeff A. Beeler (2017) High fructose corn syrup induces metabolic dysregulation and altered dopamine signaling in the absence of obesity. In: Plos onehttps://doi.org/10.1371/journal.pone.0190206
      • “We confirm prior studies demonstrating that HFCS [high fructose corn syrup] can induce metabolic dysregulation and add to accumulating data that this can arise in the absence of obesity. Reduced dopamine is associated with obesity and may contribute to compulsive eating. We demonstrate that HFCS can impair dopamine function in the absence of weight gain or increased fat consumption. As reduced dopamine function has been implicated in compulsive behaviors and reduced energy expenditure and insulin dysregulation incurs increased obesity risk, changes in glucose regulation and dopamine function induced by HFCS may precede and contribute to obesity in the long-run.”
    • Katie Page et al. (2013) Abdominal fat is associated with a greater brain reward response to high-calorie food cues in Hispanic women. In: Obesity (Silver Spring). 2013 Oct;21(10): 2029-36. doi: 10.1002/oby.20344. Epub 2013 May 29.
      • Exposure to high-calorie foods promotes overeating by stimulating brain reward pathways and appetite. Interpretation on Page’s homepage: “Dr. Page and team found that obese young adults reported more hunger and a greater desire to eat when they viewed pictures of high-calorie foods such as chocolate cake … These images triggered the appetite and reward centers in the brain, and these neural and behavioral responses to high-calorie food stimuli may promote eating.”
    • Katie Page et al. (2013) Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways. In: JAMA. 2013 Jan 2;309(1): 63-70. doi: 10.1001/jama.2012.116975.
      • Study on neurophysiological factors that might underlie associations between fructose consumption and weight gain. Interpretation: see Page, 2015 and the Page’s homepage: “These findings suggest that while glucose suppresses brain activity in regions that promote the desire to eat, fructose may promote overeating through its inability to effectively suppress the desire to seek out food”.
    • Katie Page (2015) Fructose, Glucose, and Your Brain. The Page Lab for Brain Regulation of Appetite Control & Eating Behavior at USC.  https://www.drkatiepage.com/2015/05/215/
      • “Our results suggest that consuming fructose relative to glucose activates brain reward regions and may promote feeding behavior. When volunteers consumed the fructose drink (compared to when they consumed the glucose drink), it led to greater activity in brain reward areas, including the orbitofrontal cortex. Moreover, fructose consumption correlated with greater ratings of hunger and desire for food, as well as a greater willingness to give up long-term money rewards to obtain immediate high-calorie foods.”

     

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